葛根素对大鼠心肌梗死后梗死部位胆碱能神经支配的影响

目的:观察葛根素对大鼠心肌梗死后梗死部位去胆碱能神经支配的影响,以求证实葛根素的神经保护作用。方法:SD大鼠28只,分为正常对照组、心肌梗死模型组、神经生长因子组和葛根素组。2d后取材,以Karnovsky-Roots法,显示胆碱能神经纤维,应用多功能真彩色病理图像分析系统分析胆碱能神经纤维密度。结果:心肌梗死模型组大鼠梗死区及梗死周围区胆碱能神经纤维密度均比正常对照组明显降低(均P<0.01);神经生长因子组和葛根素组大鼠胆碱能神经纤维密度均比模型组明显增高(均P<0.05);葛根素组与神经生长因子组比较无明显差别(P>0.05)。结论:葛根素…     

注射用鼠神经生长因子对大鼠缺血脑组织神经生长因子及脑源性神经营养因子表达的影响

目的研究注射用鼠神经生长因子对大鼠缺血脑组织中脑源性神经营养因子(BDNF)和神经生长因子(NGF)表达的影响。方法健康雄性Wistar大鼠,采用改良的Zea-Longa法建立大脑中动脉局灶缺血模型(MCAO)。实验分为模型对照组和注射用鼠神经生长因子组,每组各20只大鼠。注射用鼠神经生长因子组予以腹腔内注射鼠神经生长因子,每天1次,每次9 k U;模型对照组每天注射等量0.9%氯化钠注射液。72 h后行神经功能评分,然后处死,分别取脑梗死周围、海马区和梗死区脑组织作免疫组织化学染色检测BDNF、NGF蛋白表达变化,原位杂交检测BDNF m RNA、NGF m RNA的表达。结果治疗3 d后注射用鼠神经生长因子组神经功能缺损评分低于模型对照组(P<0.05)。注射用鼠神经生长因子治疗组BDNF和NGF蛋白、BDNF m RNA和NGF m RNA在梗死区周围和海马区表达均高于模型对照组,差异有统计学意义(P<0.05),在梗死区差异均无统计学意义(P>0.05)。结论注射用鼠神经生长因子可上调大鼠梗死区周围和海马区缺血脑组织中BDNF和NGF的表达,并可能通过此机制起到保护作用。     

大鼠心肌梗死后非梗死区基质重构及相关调节因子变化的研究

目的:探讨大鼠急性心肌梗死后非梗死区心肌基质重构的机制及相关调节因子的变化。方法:结扎左冠状动脉前降支制作大鼠心肌梗死模型,分别于造模后1、3、7、14和28d处死动物,采用Masson染色检测非梗死区心肌胶原容积分数(CVF),明胶酶谱法检测基质金属蛋白酶(MMP)-2、金属蛋白酶组织抑制剂(TIMP)-2的活性,实时荧光定量PCR法检测核转录因子(NF)-κBmRNA、肿瘤坏死因子(TNF)-αmRNA表达。结果:与假手术组相比较,心肌梗死组大鼠非梗死区CVF随梗死后时间的延长而增加,28d最明显(P<0.01);MMP-2、TIMP-2活性随时间延长而增加,二者在梗死后14d达高峰,后有所下降,28d时活性仍高于假手术组(P<0.05);TNF-α的表达于梗死后7d达高峰(P<0.01),后有所下降,持续到28d仍高于假手术组(P<0.05);NF-κB的表达活性随梗死时间的延长而增加(P<0.05或P<0.01)。结论:急性心肌梗死后心肌非梗死区MMP-2/TIMP-2及相关调节因子活性改变具有明显时间依从性,是导致非梗死区基质重构的机制之一。     

丁苯酞软胶囊对脑缺血痴呆大鼠记忆能力的影响

目的观察丁苯酞软胶囊(dl-3n-butylphthalide,NBP)对脑缺血(cerebral infarction,CI)大鼠学习记忆能力的影响。方法 SD大鼠随机分为正常组、假手术组、模型组、治疗组与对照组。采用自体血栓法制作CI痴呆(vascular dementia VD)模型。治疗组采用NBP灌胃,对照组采用尼莫地平治疗,给药时间30 d。模型组、假手术组和正常组均给予生理盐水灌胃。治疗后以Morris水迷宫检测其学习记忆行为能力,HE染色检测梗死灶周围组织形态学改变。结果 Morris水迷宫实验中,与正常组比较,模型组大鼠逃避潜伏期明显延长(P<0.05),平均探索次数显著减少(P<0.05);与模型组比较,治疗组、对照组大鼠逃避潜伏期明显缩短(P<0.05),平均探索次数显著增加(P<0.05)。光镜观察显示,与模型组相比,治疗组和对照组均可见海马CA1区神经元数目明显增多,变性坏死细胞减少。结论 NBP可以改善VD大鼠学习记忆能力,其机制可能与抑制CI区细胞凋亡,保护海马CA1区细胞有关。NBP对CI后神经细胞有明显保护作用。     

葛根素对急性脑缺血模型大鼠脑细胞损伤后HSP70及Fas蛋白表达的干预作用研究

目的:探讨葛根素对急性脑缺血模型大鼠脑细胞损伤后热休克蛋白70(HSP70)及Fas蛋白表达的干预作用机制。方法:将12只急性脑缺血模型大鼠随机分为单纯缺血组(生理盐水)和葛根素干预组,各6只,每只大鼠再分别按缺血侧(实验组)和非缺血侧(对照组)进行自身对照,用HE染色及免疫组织化学SP法测定HSP70表达情况;另将脑缺血模型大鼠随机分为对照组(生理盐水、缺血侧)、葛根素干预组(缺血侧)、正常组(非缺血侧),各6只,用HE染色及免疫组织化学SP法测定Fas表达情况。结果:单纯缺血对照组及葛根素干预对照组HSP70呈阴性或弱阳性表达,而在单纯缺血实验组及葛根素干预实验组中HSP70均表达增强(P<0.01),葛根素干预实验组的表达则明显强于单纯缺血实验组(P<0.01);Fas蛋白在各组中均有不同程度的表达,阳性细胞绝大部分为神经元,以锥体细胞表达强度最强,各组间阳性细胞数均无显著差异(P>0.05);HE切片中,对照组和葛根素组死亡细胞数均明显多于正常组(P<0.01),且对照组明显多于葛根素组(P<0.01)。结论:葛根素对急性脑缺血损伤具有保护作用,主要通过上调HSP70的表达来实现,而与Fas蛋白的表达及细胞凋亡等相关不强。     

迷走神经对大鼠肝脏葡萄糖代谢和纤维化的影响

目的:研究迷走神经对于大鼠肝脏葡萄糖代谢和肝纤维化形成的影响。方法:（1）建立去迷走神经肝脏模型,SD大鼠32只分模型组及对照组,每组16只。模型组切除迷走神经肝支,对照组仅行开腹神经探查手术。术后每周各采集1次肝脏组织标本,每次4只,连续4周。标本进行VAChT免疫组化,观察肝脏胆碱能神经纤维的表达情况。（2）肝糖原及肝纤维化指标测定.SD大鼠32只分为实验空腹、实验进食及对照空腹和对照进食4组,各8只。实验组行迷走神经肝支切除,对照组行开腹神经探查手术。各组分别测定肝糖原,以及肝组织HA、LN、PC Ⅲ和CIV含量。结果:模型组去迷走神经3周后肝胆碱能神经明显减少,第4周基本消失。实验组空腹肝糖原含量显著低于对照组（P<0.01）,且进食后亦无明显变化（P<0.05）,而对照组进食后肝糖原增加显著（P<0.01）。实验组HA、LN、PC Ⅲ和CIV含量明显高于对照组（P<0.01或P<0.05）。结论:大鼠去除迷走神经后4周,能够达到完全去神经肝脏状态,肝脏去迷走神经后葡萄糖的合成和储存能力显著降低,去神经后肝脏的抗纤维化能力明显减弱。     

葛根素对STZ诱导的糖尿病大鼠视网膜的保护作用及机制研究

目的探讨葛根素对糖尿病大鼠视网膜的保护作用及可能机制。方法 40只♂SD大鼠随机分为正常对照组、糖尿病(DM)模型组、DM+葛根素低剂量组(Pue1组)、DM+葛根素高剂量组(Pue2组)。给药后4周,行视网膜组织病理学检查,荧光法检测视网膜晚期糖基化终末产物(ad-vanced glycation end products,AGEs)含量、Real-time PCR法、Western blot法分别检测视网膜组织晚期糖基化终末产物受体(receptor of advanced glycation end products,RAGE)、血管内皮生长因子(vascular endothelial growth factor,VEGF)mR-NA表达和蛋白水平。结果 DM组视网膜外核层细胞厚度明显变薄,Pue2组较DM组有所好转。DM大鼠视网膜中VEGF的mRNA和蛋白表达水平均明显高于正常对照组(P<0.01);Pue1、Pue2组VEGF的mRNA和蛋白表达水平均明显下降(P<0.01)。DM大鼠视网膜内AGEs水平较正常对照组明显上调(P<0.05),高剂量葛根素能抑制AGEs形成(P<0.05)。RT-PCR与Western blot结果显示,DM大鼠视网膜中RAGE的mRNA水平和蛋白表达均高于正常对照组(P<0.05),高剂量葛根素可使之下调(P<0.05)。结论葛根素可抑制DM大鼠视网膜AGEs形成及RAGE的表达,抑制视网膜VEGF的表达,起到保护糖尿病大鼠视网膜的作用。     

EPO和CEPO对心肌梗死大鼠梗死面积和血管新生的作用的比较

目的:探讨氨甲酰促红细胞生成素(CEPO)和促红细胞生成素(EPO)对心肌梗死大鼠梗死面积和新生血管的作用。方法:购置SD大鼠40只为研究对象,随机取SD大鼠10只设为空白对照组,剩余30只SD大鼠采用左冠状动脉结扎诱导大鼠发生急性心肌梗死动物模型,建模后随机分为模型对照组、EPO组和CEPO组。空白对照组和模型对照组在相同时期给予相同剂量的生理盐水耳缘静脉注射,CEPO组耳缘静脉注射CEPO(每周2次,单次注射剂量为50ug/kg),EPO组耳缘静脉注射EPO(注射剂量为0.3mg/kg),比较各组梗死面积、血管新生数量、血流动力学参数。结果:CEPO组干预后1个月LVSP、+dp/dtmax、-dp/dtmax水平均高于模型对照组和EPO组(P0.05);LVDP水平低于模型对照组和EPO组(P0.05);CEPO组干预后1个月梗死面积均小于模型对照组和EPO组(P0.05);EPO组干预后1个月梗死面积小于模型对照组(P0.05);免疫组化结果表明:EPO组干预后1个月血管新生数量多于模型对照组但少于CEPO组(P0.05)。结论:EPO和CEPO均能减少心肌梗死大鼠面积,但是后者效果更佳,能改善病灶部位血流动力学水平,可能与血管新生有关。     

葛根素对糖尿病大鼠视网膜的保护及对NF-κB表达的抑制

目的探讨糖尿病(DM)大鼠视网膜功能、超微结构的变化和NF-κB的表达及葛根素的干预作用。方法采用单次ip给予链脲佐菌素(STZ)60 mg·kg-1制备DM模型。ig给予葛根素125,250和500mg·kg-1组,连续给药4周。视网膜电图(ERG)测定视网膜功能、透射电镜观察视网膜超微结构、TUNEL法检测视网膜细胞凋亡以及免疫组织化学染色法检测视网膜组织NF-κB p65活性。结果与正常对照组相比,DM模型组ERG的b波振幅明显降低。与DM模型组相比,葛根素250和500 mg·kg-1组的b波振幅明显上升(P<0.05);透射电镜下见DM模型组视网膜神经节细胞,内、外核层细胞均出现线粒体改变。葛根素干预后超微结构改变明显好转。与正常对照组相比,DM模型组视网膜细胞凋亡指数显著增高以及NF-κB p65表达明显增强,葛根素干预后各组凋亡指数均显著下降,葛根素250和500 mg·kg-1组NF-κB p65表达显著下降(P<0.05)。结论 DM大鼠早期即出现神经视网膜功能和超微结构的改变,葛根素可抑制NF-κB的活化,抑制视网膜神经细胞的凋亡从而起到保护神经视网膜的作用。     

葛根素对大鼠脑缺血再灌注后Caspase-3表达的影响

目的:研究葛根素对缺血再灌注大鼠海马神经元Caspase-3表达的影响。方法:用插线法制作大鼠大脑中动脉闭塞(middlecerebralarteryocclusion,MCAO)局灶性脑缺血再灌注模型,左侧MCAO1h,再灌注23h后处死,对照组给予生理盐水,葛根素组给予葛根素。苏木精-伊红染色观察缺血侧海马区组织形态学改变,海马区Caspase-3的表达通过免疫组化来测定。结果:对照组、葛根素组、假手术组缺血侧海马区平均密度值分别为0.13±0.01、0.07±0.01、0.05±0.01。对照组大鼠缺血侧海马区Caspase-3的表达较假手术组显著增强(P<0.01),给予葛根素处理后,Caspase-3的表达减弱(P<0.01)。对照组缺血侧海马区许多神经元有凋亡现象,葛根素组凋亡神经元减少,假手术组偶见凋亡神经元。结论:脑缺血再灌注损伤可致海马区Caspase-3的表达增加,凋亡神经元增多。葛根素可下调海马区Caspase-3的表达,抑制神经元的凋亡,对脑组织可能有保护作用。     

葛根素联合牛磺酸对2型糖尿病大鼠胰腺的保护作用

目的:探讨葛根素联合牛磺酸对2型糖尿病大鼠胰腺的保护作用。方法:将成模的40只Wistar大鼠随机分为糖尿病组(DM组)、单用牛磺酸组(Tau组)、单用葛根素组(Pue组)和葛根素联合牛磺酸组(Pue+Tau组)。8周后,测4组大鼠糖化血红蛋白(HbA1c)、血浆葡萄糖(Glucose)、胰岛素(Insulin)、超氧化物歧化酶(SOD)、丙二醛(MDA)、活性氧(ROS)及胰腺线粒体MDA、ROS及SOD,免疫组织化学方法检测各组大鼠胰腺组织胰十二指肠同源盒基因1(PDX-1)的表达。结果:Tau组、Pue组及Pue+Tau组较DM组大鼠血浆SOD活性和血浆胰岛素水平均有显著升高,而Glucose、MDA、ROS及HbA1c呈不同程度的降低;并且3个给药组大鼠胰腺线粒体MDA和ROS含量较DM组均有不同程度的降低,而SOD活性均有显著升高,其中Pue+Tau组这种变化更加明显;免疫组织化学染色显示DM组大鼠胰岛细胞中PDX-1表达水平较低,Tau和Pue组胰岛细胞PDX-1表达上调,Pue+Tau组PDX-1表达明显上调。结论:葛根素联合牛磺酸对2型糖尿病大鼠胰腺有保护作用,其机制可能与降低氧化应激水平,上调PDX-1基因表达有关。     

Puerarin pretreatment attenuates cardiomyocyte apoptosis induced by coronary microembolization in rats by activating the PI3K/Akt/GSK-3β signaling pathway

Coronary microembolization (CME) is associated with cardiomyocyte apoptosis and cardiac dysfunction. Puerarin confers protection against multiple cardiovascular diseases, but its effects and specific mechanisms on CME are not fully known. Hence, our study investigated whether puerarin pretreatment could alleviate cardiomyocyte apoptosis and improve cardiac function following CME. The molecular mechanism associated was also explored. A total of 48 Sprague-Dawley rats were randomly divided into CME, CME + Puerarin (CME + Pue), sham, and sham + Puerarin (sham + Pue) groups (with 12 rats per group). A CME model was established in CME and CME + Pue groups by injecting 42 μm microspheres into the left ventricle of rats. Rats in the CME + Pue and sham + Pue groups were intraperitoneally injected with puerarin at 120 mg/kg daily for 7 days before operation. Cardiac function, myocardial histopathology, and cardiomyocyte apoptosis index were determined via cardiac ultrasound, hematoxylin-eosin (H&E) and hematoxylin-basic fuchsin-picric acid (HBFP) stainings, and TdT-mediated dUTP nick-end labeling (TUNEL) staining, respectively. Western blotting was used to measure protein expression related to the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/glycogen synthase kinase-3β (GSK-3β) pathway. We found that, puerarin significantly ameliorated cardiac dysfunction after CME, attenuated myocardial infarct size, and reduced myocardial apoptotic index. Besides, puerarin inhibited cardiomyocyte apoptosis, as revealed by decreased Bax and cleaved caspase-3, and up-regulated Bcl-2 and PI3K/Akt/GSK-3β pathway related proteins. Collectively, puerarin can inhibit cardiomyocyte apoptosis and thus attenuate myocardial injury caused by CME. Mechanistically, these effects may be achieved through activation of the PI3K/Akt/GSK-3β pathway.     

Regulation of cardiac nerves: a new paradigm in the management of sudden cardiac death?

The heart is extensively innervated, and its performance is tightly regulated by the autonomic nervous system. To maintain cardiac function, innervation density is stringently controlled, being high in the subepicardium and the central conduction system. In diseased hearts, cardiac innervation density varies, which in turn leads to sudden cardiac death. After myocardial infarction, sympathetic denervation is followed by reinnervation within the heart, leading to unbalanced neural activation and lethal arrhythmia. Diabetic sensory neuropathy causes silent myocardial ischemia, characterized by loss of pain perception during myocardial ischemia, which is a major cause of sudden cardiac death in diabetes mellitus (DM). Despite its clinical importance, the molecular mechanism underlying innervation density remains poorly understood. We found that cardiac sympathetic innervation is determined by the balance between neural chemoattraction and chemorepulsion, both of which occur in the heart. Nerve growth factor (NGF), which is a potent chemoattractant, is synthesized abundantly by cardiomyocytes and is induced by endothelin-1 upregulation in the heart. In contrast, Sema3a, which is a neural chemorepellent, is expressed strongly in the trabecular layer in early stage embryos and at a lower level after birth, leading to epicardial-to-endocardial transmural sympathetic innervation patterning. We also found that cardiac NGF downregulation is a cause of diabetic neuropathy, and that NGF supplementation rescues silent myocardial ischemia in DM. Both Sema3a-deficient and Sema3a-overexpressing mice showed sudden death or lethal arrhythmias due to disruption of innervation patterning. The present review focuses on the regulatory mechanisms involved in neural development in the heart and their critical roles in cardiac performance.     

Puerarin from Pueraria lobate attenuates ischemia-induced cardiac injuries and inflammation in vitro and in vivo: The key role of miR-130a-5p/HMGB2 pathway

Acute myocardial infarction (AMI) is a common cardiovascular disease and puerarin (Pue) is an active compound from Pueraria lobate with cardio-protective potential. In the current study, the mechanism underlying the cardio-protective effects of Pue was explored by focusing miR-130a-5p/HMGB2 pathway. MiR expression profile was determined and myocardial infarction was induced in cardiomyocytes and rats, which was treated with Pue. The role of miR-130a-5p and downstream HMGB2/NF-κB axis in the cardio-protective effects of Pue was also explored. Pue increased viability and suppressed inflammation in OGD cardiomyocytes, which was associated with the deactivation of HMGB2/NF-κB pathway. After the suppression of miR-130a-5p, the cardio-protective effects of Pue were compromised. In rat models, Pue attenuated structure deterioration and inflammatory response in heart. At the molecular level, miR-130a-5p was up-regulated, and HMGB2 were down-regulated. It was demonstrated that Pue induced the expression of miR-130a-5p, which suppressed the activity of HMGB2/NF-κB, contributing to the attenuation of infarct heart tissues.     

葛根素预防压力过载性心脏肥大的保护作用及机制

目的研究葛根素对心脏肥大大鼠的保护作用,并探讨其相关机制。方法将主动脉缩窄术(降主动脉结扎,aortic banding,AB)所致心脏肥大的40只雄性Spraguee Dawley大鼠(体质量80~100g),分为阳性对照组(control组)、假手术组(shamoperated,SO组)、葛根素组(Pue组)和雷帕霉素组(RAPa组)。检测各组经相应药物治疗后,腺苷酸活化蛋白激酶(5′-adenosine monophosphate kinase,AMPK)的活性及自噬功能。同时,体外检测异丙肾上腺素和3-甲基腺嘌呤所致的心肌影响。结果葛根素组治疗3周后,大鼠明显恢复自噬;葛根素治疗6周后,有效地限制大鼠心脏细胞肥大和细胞凋亡。雷帕霉素组具有相似作用。体外研究,葛根素对异丙肾上腺素所致的H9c2细胞也具有类似的抗肥大和抗细胞凋亡作用。用3-甲基腺嘌呤预处理H9c2细胞,抑制自噬功能后,葛根素的保护作用被阻断。结论葛根素通过AMPK/mTOR信号途径,部分恢复细胞自噬功能,发挥抗心脏细胞肥大和抗细胞凋亡作用。     

不同剂量葛根素预处理对兔急性心肌缺血／再灌注损伤时心梗范围及心肌IL-6、TNF—α的影响

目的观察不同剂量葛根素预处理对兔心肌缺血再灌注心肌的保护作用。方法新西兰大白兔60只。随机分为5组,分别测定心肌梗死范围、心肌TNF—α、IL-6。结果与对照组相比,经葛根素与/或氟伐他汀预处理组心梗面积明显减少（P〈0．01）,IL-6、TNF—α含量明显减少（P〈0．01）。结论兔急性心梗再灌注时非梗死区心肌IL-6、TNF—α浓度升高：葛根素短期预处理可以抑制炎症反应,减少心梗体积比;氟伐他汀短期预处理抑制炎症反应,减少心梗体积比作用大于葛根素：葛根素联合氟伐他汀短期预处理抑制炎症反应．减少心梗体积比作用大于单用葛根素或氟伐他汀。     

四氢生物蝶呤对大鼠急性心肌缺血再灌注损伤的保护作用及其机制研究

目的研究四氢生物蝶呤对大鼠急性心肌缺血再灌注损伤的保护作用,并探讨其作用机制。方法 Wistar大鼠随机分为对照组、假手术组、模型组及四氢生物蝶呤5、10 mg/kg组,每组10只。结扎左冠状动脉前降支,制备急性心肌缺血再灌注损伤模型。对照组、假手术组和模型组均ig生理盐水2 mL,四氢生物蝶呤组ig四氢生物蝶呤5、10 mg/kg。1次/d,连续给药14 d。导管法测定血流动力学指标:左心室舒张最大速率(-dp/dtmax)、左心室舒张期末压(LVEDP)、左室开始收缩至左室内压上升速率峰值时间(Tau);ELISA法测定血浆脑钠素(BNP)活性;按试剂盒说明测定心肌一氧化氮合酶(eNOS)活性、NO生成量;染色法测定心肌梗死面积,计算心肌梗死程度;免疫组化法测定β3水平。结果与模型组比较,四氢生物蝶呤5、10 mg/kg组-dp/dtmax显著增高,LVEDP显著降低,Tau明显缩短,差异均具有统计学意义(P0.05、0.01);血浆BNP显著下降,eNOS活性、NO生成量均显著升高(P0.01);心肌梗死面积更小,心肌梗死程度更轻(P0.01);β3表达水平升高(P0.01)。结论四氢生物蝶呤可以减少急性缺血再灌注损伤大鼠心肌梗死面积,改善心肌舒张功能,对大鼠急性缺血再灌注损伤具有保护作用,可能与激活eNOS活性、提高NO生成量和β3受体有关。     

槲皮素对心肌缺血再灌注损伤的保护作用及机制研究

目的探讨槲皮素(QU)对心肌缺血再灌注(MI/R)损伤的保护作用及其作用机制。方法采用结扎左冠脉前降支30 min再灌注2 h的方法复制MI/R损伤大鼠模型,随机分为假手术组、模型组、QU组(25、50、100 mg/kg),每组10只,各组于术前1周开始灌胃给药,1次/d。再灌注后取心脏,染色法测定心肌梗死面积;免疫组化法测定心肌组织NF-κB和ICAM-1表达情况;取心肌匀浆,髓过氧化物酶(MPO)法测定中性粒细胞浸润情况。结果QU高、中剂量可分别缩小心肌梗死面积至25.00%、25.31%,与模型组(32.55%)比较差异有统计学意义(P<0.05);QU各剂量组心肌MPO活力分别降低至185.70、190.66、210.03 U/g,与模型组(311.72 U/g)比较差异均有统计学意义(P<0.05,P<0.01);QU各剂量组心肌组织ICAM-1阳性区面积百分比分别降至32.08%、32.65%、36.42%,与模型组(42.67%)比较差异有统计学意义(P<0.05,P<0.01);QU高、中剂量可使心肌NF-κB的表达水平分别降低至55.23%、54.90%,与模型组(61.05%)比较差异有统计学意义(P<0.05)。结论QU预处理可保护MI/R所致心肌损伤,其机制与抑制中性粒细胞浸润、下调NF-κB和ICAM-1的表达等有关。     

Puerarin alleviates skeletal muscle atrophy in type 1 diabetic rats

OBJECTIVE Puerarin is an important isoflavone component of traditional Chinese medicine Pueraria lobata and has a wide range of pharmacological effects.Studies have shown that puerarin has a significant alleviation effect on diabetes and its complications. This article investigates the therapeutic effect of puerarin on rat skeletal muscle atrophy caused by type 1 diabetes. METHODS SD rats were fed adaptively for 1 week, then 10 rats were randomly divided into normal control group.The rest were injected intraperitoneally with 65 mg·kg~(-1) streptozotocin(STZ). Blood was taken from the tip of the tail after 1 week and rats with fasting blood glucose levels above 16.5 mmol · L~(-1) were chosen as type 1 diabetic rats, which randomly divided into two groups: diabetic model control group and puerarin administration group(n=10). The administration group was treated with orally administration of puerarin at 100 mg·kg~(-1)·d~(-1), while the normal control group and the diabetic model group were treated with corresponding dose of normal saline. At the end of the 8-week treatment, diabetes related indicators were detected including body weight, food-intake, fasting blood glucose and glucose tolerance test. Meanwhile,skeletal muscle atrophy correlative indicators like foreleg tensile force, time of wire hanging, persistent time on sloping plate, area of skeletal muscle and atrophy markers(F-box protein 32, Fbxo32 and tripartite motif containing63, Trim63) were also detected. RESULTS Puerarin(100 mg · kg~(-1)) can lighten body weight and decrease food-intake of type 1 diabetic rats induced by STZ(P<0.05). But there was no significant amelioration in glucose tolerance and fasting blood glucose level. As for skeletal muscle strength, puerarin can significantly enhance the foreleg tensile force(P<0.01), time of wire hanging(P<0.05) and persistent time on sloping plate(P<0.01).Besides, puerarin also showed a significant effect on enhancing the area of skeletal muscle(P<0.01)while reducing expressions of Fbxo32 and Trim63(P<0.01).CONCLUSION These results suggested that 100 mg·kg~(-1) puerarin administered orally for 8 weeks could remarkably mitigate skeletal muscle atrophy, enhance musculararea and strength in type 1 diabetic rats induced by STZ.